Neonatal Neurology Neupsy Key anoxia meaning

The clinical presentation of IVH varies depending on severity. Grade I IVH is usually asymptomatic. Many grade II and some III hemorrhages are clinically silent, but there may be a saltatory course evolving over hours to days, characterized by nonspecific findings of altered level of consciousness, hypotonia, eye movement changes, subtle changes in movement, decreased spontaneous movements, and disturbed respiratory function. Some grade III hemorrhages produce hydrocephalic symptoms of varying severity, and if seen in combination with PVHI, there may be signs of severe apnea, bradycardia, extensor posturing, and opisthotonus.


There also may be flaccid weakness, cranial nerve abnormalities including fixed pupils to light, most likely leading to unresponsiveness and death within hours.Anoxia meaning there may be clonic limb movements, which some clinicians have labeled as seizures, although there is usually little electroencephalogram (EEG) correlation. Most infants who die have other lesions, such as periventricular leukomalacia (see the section “periventricular leukomalacia”), brain stem necrosis, or cerebellar necrosis.

In general, no treatment is needed for grade I and II hemorrhages, although they should be followed for progression by regular cranial ultrasonography. For grade III hemorrhage or PVHI, ongoing monitoring should be performed, with weekly head ultrasounds with daily head circumference measurement and frequent clinical assessment for increased intracranial pressure (ICP).Anoxia meaning if there is evidence of significant lateral ventricular dilatation or increased ICP, intervention may be needed. Serial lumbar punctures can be done, although they should be coupled with cranial ultrasonography to ensure that there is a resultant decrease in ventricular size. As a temporizing measure, ventricular drainage with a direct extraventricular drain or with a subcutaneous drain to a subcutaneous reservoir or a ventriculosubgaleal shunt may be helpful. Usually, if a drain is needed, eventually, a permanent ventricular shunt, usually a ventriculoperitoneal shunt, will be needed, although a third ventriculostomy may be effective as well in some cases. Every attempt should be made to delay shunting until the newborn attains as much somatic growth as possible.Anoxia meaning

TABLE 132.1 intraventricular hemorrhage clinical features, treatment, and outcome

IVH grade

Clinical syndrome

Treatment

Outcome

I

II

Usually asymptomatic

Frequently asymptomatic, may display subtle neurologic signs affecting mental status, tone, eye or muscle movements, or respiration

Follow clinically and with cranial ultrasound.

Usually normal; may have long-term behavioral/learning problems if low birth weight

III

PVHI

May show signs of hydrocephalus; may show other neurologic signs similar to grade II

May show more severe neurologic signs including apnea, bradycardia, opisthotonus, posturing

If signs of increased intracranial pressure, may require intervention: serial lumbar punctures, ventricular drainage, ventricular shunt, or third ventriculostomy

anoxia meaning

20% mortality; 75% show PHH. May progress to developmental delay, cerebral palsy, bilateral deafness, especially with bilateral blindness associated with more severe bleeds and extreme prematurity. May be normal if small hemorrhage.

IVH, intraventricular hemorrhage; PHH, posthemorrhagic hydrocephalus; PVHI, periventricular hemorrhagic infarction.

On a cellular and molecular level, hypoxia-ischemia acutely causes neuronal loss in the cerebral sulci, often with edema and infarction. Chronically, there is neuronal loss and astrocytosis, with possible atrophy, cystic encephalomalacia, ulegyria, status marmoratus, and cerebellar atrophy. Energy failure from hypoxia stems from loss of mitochondrial function, which can be confirmed by measuring increased lactic acid levels in the CSF or by magnetic resonance spectroscopy (MRS).Anoxia meaning there is accompanying membrane depolarization and an increase in neurotransmitter release, as well as excessive activation of glutamate receptors. Resultant is excitotoxic cellular injury, leading to an increase in intracellular calcium that leads to a cascade of pathologic pathways leading to secondary cell death. In addition, there is oxidative stress, which produces reactive oxygen species and subsequent reactive nitrogen radicals, also contributing to cell toxicity. After the anoxic insult, many cells undergo reoxygenation and reperfusion. Reperfusion contributes further to oxidative stress by producing more reactive oxygen species and further cellular injury.

HIE initially presents with low apgar scores, which translate into bradycardia, depressed respiration, diminished responsiveness, and decreased muscle tone ( table 132.2).Anoxia meaning one of three clinical patterns then evolves: (1) mild: awake, irritable, hyperalert, with jitteriness, dilated pupils, increased deep tendon reflexes, and normal muscle tone; (2) moderate: lethargy with depressed deep tendon reflexes, frequently with seizures; and (3) severe: apathy, with severe hypotonia, poorly reactive pupils, an absent moro reflex, depression or coma, and seizures. There is usually clinical improvement with the mild and moderate cases as the newborns become more alert, improve their tone, and are able to feed. Seizures or therapy for seizures may delay recovery. Newborns with severe encephalopathy will usually become stuporous; develop frequent seizures, respiratory depression, or brain stem abnormalities; and may show signs of decerebration.Anoxia meaning they become unresponsive and lose sucking reflexes and the moro response, and even with vigorous supportive and anticonvulsant therapy, 20% to 30% of these newborns die. If the neonate survives, seizures usually stop after 48 to 72 hours, and there is usually some recovery.

Certain patterns of brain injury seen in neuroimaging of late preterm or term infants are commonly seen in HIE, including parasagittal injury in an arterial watershed distribution and/or injury to the deep gray nuclei ( figs. 132.2 and 132.3). Neuroimaging, alternatively, may reveal another cause of encephalopathy, such as a developmental brain malformation or a focal area of infarction. Brain MRI is the most sensitive imaging modality for most lesions and usually yields the most useful information, although it requires transport, monitoring, and support.Anoxia meaning MRS, if available, can be useful for diagnosis of HIE if a lactate peak is seen. Head CT is useful for detecting intracranial hemorrhage and brain calcifications but is less sensitive for detecting mild brain edema or white matter injury, which is somewhat obscured because of the high water content of the newborn white matter. The posterior fossa is not adequately imaged with CT because of bony artifact. Cranial ultrasonography can be done at the bedside but is not very sensitive for detection of white matter abnormalities or lesions in the outer cerebral cortex.

Because multiple organ systems are involved in addition to the brain, management and therapeutic measures include maintenance of physiologic homeostasis, including providing adequate ventilation, maintenance of perfusion and metabolism, avoidance of brain edema, and seizure control.Anoxia meaning therapeutic hypothermia has been shown in multiple randomized controlled trials to lower mortality and major neurodevelopmental disability in term

And late preterm infants with moderate or severe HIE [ level 1]. 1 there are some adverse effects of hypothermia, including an increase in sinus bradycardia and in thrombocytopenia, but the benefits of cooling outweigh these short-term adverse effects. Questions still remaining are the optimal timing of the cooling after birth (research protocols have started cooling before 6 hours of age), the duration of cooling needed (most research protocols have cooled for 72 hours), the level of hypothermia required, and the method (selective head cooling vs.Anoxia meaning whole body cooling).

TABLE 19.2 distinguishing features of the three clinical stages of hypoxic-ischemic encephalopathy in the full-term newborn

@@

Stage 1

Stage 2

Stage 3

Level of consciousness

Hyperalert

Lethargic or obtunded

Stuporous

Neuromuscular control

Muscle tone

Normal

Mild hypotonia

Flaccid

Posture

Mild distal flexion

Strong distal flexion

Intermittent decerebration

Stretch reflexes

Overactive

Overactive

Decreased or absent

Segmental myoclonus

Present

Present

Absent

Complex reflexes

Suck

Weak

Weak or absent

Absent

Moro

Strong: low threshold

Weak, incomplete, high threshold

Absent

Oculovestibular

Normal

Overactive

Weak or absent

Tonic neck

Slight

Strong

Absent

Autonomic function

Generalized sympathetic

Generalized parasympathetic

anoxia meaning

Both systems depressed

Pupils

Mydriasis

Miosis

Variable; often unequal; poor light reflex

Heart rate

Tachycardia

Bradycardia

Variable

Bronchial and salivary secretions

Sparse

Profuse

Variable

Gastrointestinal motility

Normal or decreased

Increased; diarrhea

Variable

Seizures

None

Common; focal or multifocal

Uncommon (excluding decerebration)

Electroencephalogram findings

Normal (awake)

Early: low-voltage continuous delta and theta

Early: periodic pattern with isopotential phases

Later: periodic pattern (awake)

Later: totally isopotential

Seizures: focal 1-1½-hz spike-and-wave

Duration

24 h

2-14 d

Hours to weeks

Sarnat HB, sarnat MS. Neonatal encephalopathy following fetal distress. A clinical and electroencephalographic study.Anoxia meaning arch neurol. 1976;33(10):696-705.